Invasive breast carcinoma - IARC

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Most melanotic tumours of the breast re p resent metastases from malignant melanomas originating in extra-mammary sites {2694}. Primary melanomas may arise anywhere in the skin of the breast, but an origin in the nipple-areola complex is extremely rare {2168}. The differential diagnosis of malignant melanoma arising in the nipple areolar region must include Paget disease, the cells of which may on occasion contain melanin pigment {2544}. This is discussed in the section on Paget disease. Genetics The genetic variation seen in breast cancer as a whole is similarly reflected in ductal NOS tumours and has until recently proved difficult to analyse or explain. The increasing accumulation of genetic alterations seen with increasing grade ( d e c reasing degree of diff e re n t i a t i o n ) has been used to support the hypothesis of a linear progression model in this type and in invasive breast cancer as a whole. The recent observation by a number of groups that specific genetic lesion or regions of alteration are associated with histological type of cancer or related to grade in the large ductal NOS group does not support this view. It implies that b reast cancer of ductal NOS type includes a number of tumours of unrelated genetic evolutionary pathways {365} and that these tumours show fundamental differences when compared to some special type tumours including lobular {1085} and tubular carcinoma {2476}. F u rt h e rm o re, recent cDNA micro a r r a y analysis has demonstrated that ductal NOS tumours can be classified in to subtypes on the basis of expression patterns {2218,2756}. Prognosis and predictive factors Ductal NOS carcinoma forms the bulk (50-80%) of breast cancer cases and its p rognostic characteristics and management are similar or slightly worse with a 35-50% 10 year survival {771} compare d to breast cancer as a whole with aro u n d a 55% 10 year survival. Prognosis is influenced profoundly by the classical p rognostic variables of histological grade, tumour size, lymph node status and vascular invasion (see general discussion of prognosis and predictive factors at the end of this chapter) and by p redictors of therapeutic response such as estrogen receptor and ERBB2 status. A Fig. 1.17 Carcinoma with choriocarcinomatous features. A,B Multinucleated tumour cells with smudged nuclei extend their irregular, elongated cytoplasmic processes around clusters of monocytic tumour cells, mimicking the biphasic growth pattern of choriocarcinoma. B Note the abnormal mitotic figures in this high grade carcinoma. Approximately 70-80% of ductal NOS breast cancers are estrogen receptor positive and between 15 and 30% of cases ERBB2 positive. The management of ductal NOS carcinomas is also influenced by these prognostic and predictive characteristics of the tumour as well as focality and position in the breast. Invasive lobular carcinoma Definition An invasive carcinoma usually associated with lobular carcinoma in situ is composed of non-cohesive cells individually dispersed or arranged in single-file linear pattern in a fibrous stroma. ICD-O code 8520/3 Epidemiology Invasive lobular carcinoma (ILC) represents 5-15% of invasive breast tumours {725,771,1780,2541,2935,3133}. During the last 20 years, a steady increase in its incidence has been reported in women over 50 {1647}, which might be attributable to the increased use of hormone replacement therapy {312,1648,2073}. The mean age of patients with ILC is 1-3 years older than that of patients with infiltrating ductal carcinoma (IDC) {2541}. Clinical features The majority of women present with a palpable mass that may involve any part of the breast although centrally located tumours were found to be slightly more common in patients with ILC than with IDC {3133}. A high rate of multicentric tumours has been reported by some {699,1632} but this has not been found in other series based on clinical {2541} or B radiological {1599} analysis (see bilateral b reast carcinoma section). An 8-19% incidence of contralateral tumours has also been reported {699,725,834}, representing an overall rate of 13.3 %. This may be higher than that for IDC {1241,2696}. However, no significant difference in the rate of bilaterality was observed in other series of cases {648, 1168,2186}. At mammography, architectural distortion is more commonly observed in ILC than in IDC whereas microcalcifications are less common in ILC {895,1780,3066}. Macroscopy ILC frequently present as irregular and poorly delimited tumours which can be d i fficult to define macro s c o p i c a l l y because of the diffuse growth pattern of the cell infiltrate {2696}. The mean diameter has been reported to be slightly larger than that of IDC in some series {2541,2696,3133}. Histopathology The classical pattern of ILC {895, 1780,3066} is characterized by a proliferation of small cells, which lack cohesion Fig. 1.18 Macroscopy of an invasive lobular carcinoma displays an ill defined lesion. Invasive breast cancer 23
A Fig. 1.19 Mammography of invasive lobular carcinoma. A Architectural distortion in the axillary tail, corresponding to a palpable area of thickening. B Magnification view of the architectural axillary distortion. B Fig. 1.20 In situ and invasive lobular carcinoma. The larger cells on the left and lower part of the field are invasive tumour cells. and appear individually dispersed through a fibrous connective tissue or arranged in single file linear cords that invade the stroma. These infiltrating cords frequently present a concentric pattern around normal ducts. There is often little host reaction or disturbance of the background architecture. The neoplastic cells have round or notched ovoid nuclei and a thin rim of cytoplasm with an occasional intracytoplasmic lumen {2312} often harbouring a central mucoid inclusion. Mitoses are typically infrequent. This classical form of ILC is associated with features of lobular carcinoma in situ in at least 90% of the cases {705,2001}. In addition to this common form, variant patterns of ILC have been described. The solid pattern is characterized by sheets of uniform small cells of lobular morphology {835}. The cells lack cell to cell cohesion and are often more pleomorphic and have a higher frequency of mitoses than the classical type. In the alveolar variant , tumour cells are mainly arranged in globular aggregates of at least 20 cells {2668}, the cell morphology and growth pattern being otherwise typical of lobular carcinoma. Pleomorphic lobular carcinoma retains the distinctive growth pattern of lobular carcinoma but exhibits a greater degree of cellular atypia and pleomorphism than the classical f o rm {808,1858,3082}. Intra-lobular lesions composed of signet ring cells or pleomorphic cells are features frequently associated with it. Pleomorphic lobular carcinoma may show apocrine {808} or histiocytoid {3047} diff e rentiation. A mixed group is composed of cases showing an admixture of the classical type with one or more of these patterns {705}. In about 5% of invasive breast cancers, both ductal and lobular features of differentiation are present {1780} (see Mixed type carcinoma, page 21). Analysis of E-cadherin expression may help to divide these cases between ductal and lobular tumours but the immunophenotype remains ambiguous in a minority of cases {34}. The admixture of tubular growth pattern and small uniform cells arranged in a linear pattern defines tubulo-lobular carcinoma (TLC) (ICD-O 8524/3) {875}. LCIS is observed in about one third of TLC. Comparison of the clinico-pathological features of TLC and pure tubular carcinoma (TC) has shown that axillary metastases were more common in TLC (43%) than in TC (12%) {1062}. A high rate of estrogen receptor (ER) positivity has also been reported in TLC {3141}. Further analysis of TLC, especially regarding E- cadherin status, should help to determine whether TLC should be categorized as a variant of tubular or of lobular tumours. Without this data these tumours are best classified as a variant of lobular carcinoma. Immunoprofile About 70-95% of lobular carcinomas are ER positive, a rate higher than the 70- 80% observed in IDC {2541,3235}. Progesterone receptor (PR) positivity is 60-70% in either tumour type {2541, A B Fig. 1.21 A Invasive lobular carcinoma. B Loss of E-cadherin expression is typical of lobular carcinoma cells. Note immunoreactivity of entrapped normal lobules. C Large number of signet ring cells and intracytoplasmic lumina (targetoid secretion). C 24 Tumours of the breast
Page 2: Previous volumes in this series Kle
Page 6 and 7: World Health Organization Classific
Page 8 and 9: Published by IARC Press, Internatio
Page 10 and 11: CHAPTER 1 Tumours of the Breast Can
Page 12 and 13: TNM classification of carcinomas of
Page 14 and 15: Invasive breast carcinoma I.O. Elli
Page 16 and 17: Rapid growth and greater adult heig
Page 18 and 19: tives, administrative and clerical
Page 20 and 21: Grade 1 - well differentiated: 3-5
Page 22 and 23: ent and this is occasionally extens
Page 26 and 27: A Fig. 1.22 A Classic invasive lobu
Page 28 and 29: yet others at 90% {97,2147}. For pr
Page 30 and 31: Fig. 1.27 Medullary carcinoma. The
Page 32 and 33: myoepithelial cells in fibro a d e
Page 34 and 35: A Fig. 1.33 Neuroendocrine carcinom
Page 36 and 37: Macroscopy Fisher et al. reported t
Page 38 and 39: Fig. 1.39 Apocrine carcinoma. Note
Page 40 and 41: cells contain intracytoplasmic lume
Page 42 and 43: A Fig. 1.50 Carcinosarcoma. A Two a
Page 44 and 45: A B C Fig. 1.75 Lobular neoplasia.
Page 46 and 47: Intraductal proliferative lesions F
Page 48 and 49: A B absence of either microcalcific
Page 50 and 51: Fig. 1.83 Atypical ductal hyperplas
Page 52 and 53: A B Fig. 1.88 Large excision biopsy
Page 54 and 55: unusual variants as well. Using thi
Page 56 and 57: esemble those identified in invasiv
Page 58 and 59: A B Fig. 1.97 Microinvasive carcino
Page 60 and 61: A Papilloma may be subject to morph
Page 62 and 63: A B C Fig. 1.103 Papillary intraduc
Page 64 and 65: colour measuring from 0.5 to 12 cm.
Page 66 and 67: Immunoprofile The cases studied by
Page 68 and 69: Glycogen-rich, clear cell carcinoma
Page 70 and 71: Differential diagnosis There may be
Page 72 and 73: quality metaphase spreads from an i
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Fig. 1.67 Lobular carcinoma of brea
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detectable distant metastasis displ
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detected at a late stage as small t
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Extent of ductal carcinoma in situ
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Benign epithelial proliferations G.
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Fig. 1.112 Microglandular adenosis.
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A Apocrine adenoma ICD-O code 8401/
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A B Fig. 1.128 Adenomyoepithelioma,
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Mesenchymal tumours M. Drijkoningen
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1113,1275}. There is a complex patt
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A B Fig. 1.137 A Lipoma. Intraparen
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Fig. 1.141 Angiosarcoma after breas
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A Fig. 1.144 Mammary osteosarcoma.
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Fibroepithelial tumours J.P. Belloc
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aged women (average age of presenta
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lished data suggests a 21% rate of
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A Fig. 1.157 Syringomatous adenoma
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Malignant lymphoma and metastatic t
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used. Inflammatory conditions in th
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male population both in the USA and
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CHAPTER 2 Tumours of the Ovary and
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Polyembryoma 9072/3 Non-gestational
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Surface epithelial-stromal tumours
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A Fig. 2.04 A Serous borderline tum
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A Fig. 2.06 Serous borderline tumou
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A Fig. 2.10 Invasive peritoneal imp
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Fig. 2.15 Mucinous carcinoma with i
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Fig. 2.20 Mucinous endocervical-lik
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A Fig. 2.28 Mucinous cystic tumour
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early secretory endometrium {2605}.
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IV, 6% {2233}. Patients with grade
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A Fig. 2.37 A This polypoid intracy
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Fig. 2.40 Endometrioid cyst with at
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1 tumours are extremely rare. Almos
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Fig. 2.50 Borderline Brenner tumour
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express thrombomodulin and have bee
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serous and transitional cell carcin
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is yellow to tan with a variable ad
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Genetic susceptibility JGCTs may pr
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Clinical features F i b romas may b
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distinguishes this tumour from the
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A Fig. 2.77 A Retiform Sertoli-Leyd
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Mean ages of 21 and 38 years and me
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Tumours unassociated with PJS form
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mal origin without crystals of Rein
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Germ cell tumours F. Nogales A. Tal
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cases, anisokaryosis has no prognos
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ation may coexist in the same neopl
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Table 2.06 Grading of ovarian immat
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A B Fig. 2.102 A Mature cystic tera
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Diagnostic procedures Elevated urin
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associated with mature teratomas sh
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atives intimately admixed. The germ
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Fig. 2.113 Mixed germ cell-sex cord
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A Fig. 2.116 A Adenomatous hyperpla
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Fig. 2.117 Small cell carcinoma, hy
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Clinical features Adenoid cystic-li
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Histopathology This epithelial tumo
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sis. Corpus luteum of pregnancy has
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Lymphomas and leukaemias L.M. Roth
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Secondary tumours of the ovary J. P
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Occasionally, the colonic adenocarc
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Peritoneal tumours S.C. Mok J.O. Sc
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A B Fig. 2.140 Cystic adenomatoid m
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whelmingly poor {1038,1547,2310}. H
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CHAPTER 3 Tumours of the Fallopian
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TNM and FIGO classification of carc
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Endometrioid adenocarcinoma Endomet
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Two examples of adenofibroma of bor
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A Fig. 3.11 Adenomatoid tumour. A T
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Clinical features Patients range in
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Fig. 3.16 Uterus-like mass. The cys
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CHAPTER 4 Tumours of the Uterine Co
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TNM and FIGO classification of non-
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Epithelial tumours and related lesi
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endometrioid adenocarcinoma fro m a
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fers from the prototypical type I e
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the ovary and bladder. Unlike prima
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schema {1535,2602}. Although this c
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Table 4.03 Altered gene function in
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Mesenchymal tumours and related les
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areas are limited to less than 30%
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A B C Fig. 4.30 Leiomyosarcoma. A T
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e used sparingly and is reserved fo
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A B Fig. 4.38 Leiomyoma with perino
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cytological atypia, tumour cell nec
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Mixed epithelial and mesenchymal tu
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Prognosis and predictive factors Th
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tumours may superficially invade th
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A Fig. 4.46 A Gestational choriocar
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A Fig. 4.49 A Classic complete hyda
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Sex cord-like, neuroectodermal and
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Secondary tumours of the uterine co
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WHO histological classification of
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Epithelial tumours M. Wells J.M. Ne
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Fig. 5.04 Mechanisms of human papil
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Fig. 5.08 Keratinizing squamous cel
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in their Asian population {2957}. I
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have a strong association with high
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e red by squamous epithelium {380}.
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endometrioid adenocarcinoma of the
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metrial epithelium. In some cases t
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with distinct cell borders and a gr
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Mesenchymal tumours M.L. Carcangiu
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{781}, liposarcoma {2840,3016}, ost
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Mixed epithelial and mesenchymal tu
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Fig. 5.44 Wilms tumour. The tumour
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A Fig. 5.47 Implant of endometrial
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CHAPTER 6 Tumours of the Vagina Alt
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Epithelial tumours E.S. Andersen A.
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Aetiology The fact that both VAIN a
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Fig. 6.10 Fibroepithelial polyp.A m
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er of mitoses varies but is usually
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ICD-O codes Adenosquamous carcinoma
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A C Fig. 6.17 Sarcoma botryoides. A
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1-11 cm. They may arise anywhere in
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elsewhere in the female genital tra
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A Fig. 6.24 Yolk sac tumour. A The
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g rowing in sheets. Some may have s
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WHO histological classification of
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Epithelial tumours E.J. Wilkinson M
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even with additional sectioning, it
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type) is a highly diff e rentiated
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Clinical features Bartholin gland c
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glandular elements surrounded by fi
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Mesenchymal tumours R.L. Kempson M.
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Table 7.03 Differential diagnosis o
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Prognosis and predictive factors A
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Table 7.04 Clark levels of cutaneou
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A Fig. 7.23 Vulvar peripheral primi
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Familial aggregation of cancers of
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BRCA1 syndrome Definition Inherited
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dispose individuals to the developm
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Fig. 8.05 To assess whether wild-ty
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Fig. 8.07 Factors that modify risk
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BRCA2 syndrome R. Eeles S. Piver S.
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tubal or ovarian carcinomas. Howeve
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in typical nuclear foci that may re
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Breast tumours Frequency Breast can
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Fig. 8.14 Codon distribution of som
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Breast tumours Age distribution and
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Hereditary non-polyposis colon canc
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essary in the evaluation of the pat
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Age distribution and penetrance Mos
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Contributors Dr Vera M. ABELER** De
Page 364 and 365:
Dr Carlo LA VECCHIA Laboratory of E
Page 366 and 367:
Dr Manuel TEIXEIRA Department of Ge
Page 368 and 369:
02.100 Dr. A. Ostor 02.101 Dr. F.A.
Page 370 and 371:
52. Akhtar M, Robinson C, Ashraf Al
Page 372 and 373:
180. Bapat K, Brustein S (1989). Ut
Page 374 and 375:
307. Bolis GB, Maccio T (2000). Cle
Page 376 and 377:
436. Chang J, Sharpe JC, A'Hern RP,
Page 378 and 379:
562. Costa MJ, Ames PF, Walls J, Ro
Page 380 and 381:
689. Di Domenico A, Stangl F, Benni
Page 382 and 383:
820. Falck J, Petrini JH, Williams
Page 384 and 385:
943. Gad A, Azzopardi JG (1975). Lo
Page 386 and 387:
1067. Grimes MM (1992). Cystosarcom
Page 388 and 389:
1197. Herod JJ, Shafi MI, Rollason
Page 390 and 391:
1323. Jacques SM, Qureshi F, Ramire
Page 392 and 393:
1449. Khalifa MA, Mannel RS, Harawa
Page 394 and 395:
1564. Lagios MD (1977). Multicentri
Page 396 and 397:
1687. Loman N, Johannsson O, Kristo
Page 398 and 399:
1807. McCluggage G, McBride H, Maxw
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1937. Mukai M, Torikata C, Iri H (1
Page 402 and 403:
2056. Norris HJ, Taylor HB (1967).
Page 404 and 405:
2180. Park JS, Jones RW, McLean MR,
Page 406 and 407:
2304. Puls LE, Hamous J, Morrow MS,
Page 408 and 409:
2 4 3 4 . Rosen PP, Groshen S, Saig
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2559. Schlesinger C, Silverberg SG
Page 412 and 413:
2686. Silverberg SG (1999). Protoco
Page 414 and 415:
2806. Stutz JA, Evans AJ, Pinder S,
Page 416 and 417:
2942. Tornos C, Silva EG, Ordonez N
Page 418 and 419:
3061. Wargotz ES, Norris HJ (1990).
Page 420 and 421:
3189. Yoshioka T, Tanaka T (2000).
Page 422 and 423:
References 425
Page 424 and 425:
Biphasic teratomas, 168 BLM, 341, 3
Page 426 and 427:
G GADD45, 343, 353 GCDFP-15, 25, 33
Page 428 and 429:
MPNST, see Malignant peripheral ner
Page 430:
Small cell / oat cell carcinoma, 32
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